- Infiltration with mononuclear cells
- Tissue destruction and repair
- New blood vessels & fibrosis
- Long duration
- Follow acute inflammation – persistence of causative agent
- Chronic from the beginning – irritants of low intensity
- Example – Tuberculosis , Johne’s disease
- Fungal diseases
- Prolonged exposure to toxic agents
- Example – Asbestos, Silica particles
Causes of chronic inflammation
- Bacteria – Pasteurella aviseptica, Erysipelothrix rhusiopathiae
- Phytotoxins – Crotalaria, senecio
- Foreign bodies – sharp objects, dust, worms, inert objects
- Constant & repeated mechanical irritation
Gross appearance
- Gray and firm, white, tough, hard (mature variety), nodules (granuloma) kidney – pitted appearance
- Smooth, dense, watery (newly formed)
- Yellowish, soft & easily cut
Microscopical appearance
- Vascular and cellular response is less
- Proliferation of fibrous connective tissue
- New blood vessel formation
- Mononuclear cells ─ predominant
- Macrophages
- Plasma cells
- Lymphocytes
- Giant cells
- Neutrophils — in bacterial infection
- Encapsulation
Chronic inflammation is characterized by
- Tissue destruction and repair
- Infiltration of macrophages, lymphocytes and plasma cells
- Formation of new blood vessels and fibrosis
- Longer duration
Two types of chronic inflammation
- This may be sequel of persistent and resolved acute inflammation
- It may develop as a slowly evolving chronic process without an acute inflammatory phase
Persistent acute inflammation
- The lesions of persistent inflammation are progressively dominated by the presence of macrophages, fibrous tissue and blood vessels e.g. Acute fibrinous pericarditis - infiltrated with fibroblasts and collagen if not resolved.
- Chronic active inflammation includes apart from neutrophils, presence of macrophages and plasma cells which may be associated with osteomyelitis, metritis and epididymitis (Brucellosis). These are mostly caused by bacteria and fungi predisposed with deficient immunocompetency.
Evolving chronic inflammation
- Diseases like tuberculosis, actinobacillosis and osteoarthritis in which chronic inflammation begins as an asymptomatic process in which neutrophils are not present but infiltrated with macrophages which deals with persistent injury. It lacks cardinal signs of acute inflammation.
Granulomatous inflammation
- This is a form of chronic inflammatory process in which aggregates of large highly activated macrophages are present. When the macrophages take up bacteria, fungi, aberrant parasite (Toxocara larva) or inert substances (silica, asbestos) which cannot be killed or fully digested, monocytes are attracted to the site that are not ineffective in phagocytosis. So that the cells continue to infiltrate the lesion and are found in large numbers. The macrophages become larger and foamy because of accumulation of causative agents, debris from an injured tissue. So this foamy macrophages are referred to as an epithelioid cells which are the hall mark of granulomatous inflammation.
- The granulomatous lesions develop slowly over a period of several weeks or months before producing clinical signs of disease. The microorganisms involved do not cause endothelial damage and are not chemoattractive, so that acute inflammatory signs and neutrophils are not seen.
Other ways of classification of chronic inflammation
- Chronic inflammation – Simple type, predominantly cellular exudates predominantly containing lymphocytes. Macrophages and plasma cells are fewer. Sometimes both lymphocytes and macrophages may predominate (lympho-histiocytic) seen in early stages of chronic inflammation like viral infection.
- Chronic active inflammation - Besides cellular components of chronic inflammation, it also contains neutrophils, fibrin and plasma protein of acute inflammatory response.
- Granulomatous inflammation - Basic cellular exudate - Predominantly activated macrophages, also epithelioid macrophages, giant cells and lesser number of lymphocytes and plasma cells. e.g. deep seated mycoses, bacterial infection with Nocardia, Brucella, Mycobacteria and protozoa
- Pyogranulomatous inflammation - This type of inflammation contains similar cellular exudates like granulomatous inflammation that multifocal infiltration of neutrophils, fibrin and plasma proteins. A nodule like granulomatous areas with neutrophils is termed as pyogranuloma e.g. Common in blastomycosis.
- Granuloma - Distinct type with well defined macrophage infiltration. Usually it can be non-caseating or caseating. Non-caseating granulomas are round to oval containing numerous macrophages, variable epithelioid macrophages, some multinucleated giant cells, peripheral zone of fibroblast, lymphocyte and plasma cells. In caseating granuloma, the centre is having grey-white, yellow pasty necrotic debris resembling cheese (Latin caseous = cheese) e.g. tuberculosis
Result of chronic inflammation
- Delayed healing
- Permanent change or scar formation
- Distortion / Disfigurement of the organ / tissue ( Inflammatory cells displace, replace or obliterate the tissue)
- Impairs mobility
- Epithelial surface – hyperplasia – Metaplasia – Neoplasia
- Increase intracranial pressure - destruction neurons and glia
Differences between acute and chronic inflammation
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Acute
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Chronic
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Short duration
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Long duration
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Irritant – Sever
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Low intensity
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Marked vascular Changes
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Less prominent
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Profuse exudate
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Scanty
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Soft in consistency
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Hard in consistency
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No fibrosis
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Proliferation of fibro vascular connective Tissue and epithelium
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Granulomatous inflammation
- Chronic inflammation
- Circumscribed lesion
- No exudates or cellular changes
The histiocytes (macrophages) in the lesion have large amount of cytoplasm and resemble epithelial cells called “EPITHELOID CELLS” . Epitheloid cells fuse to form “Giant Cells” Foreign body giant cell .e.g. Langhan’s cell
Causes for granulomatous inflammation
- Bacteria – TB, JD, Actinomyces, Actinobacillus
- Fungus – Aspergillus fumigatus
- Foreign bodies – Silica, asbestos, inert material
Result
- Helps in localising the infection
- Allows inflammatory and immune mechanism to act for longer periods of time
Allergic inflammation
- Animal / person previously sensitized to foreign bodies
- Diagnosis of JD, TB, Glanders
Sensitized animal
↓
Injection of protein (Antigen)
↓
24hours − Neutrophils / oedema
↓
48hours − Number of neutrophils - ↓ neutrophils, ↑ eosinophils / macrophages
↓
72hours − Hot, painful diffuse swelling
↓
Subsides
Viral inflmmation
- Obligatory parasites
- Cannot survive outside the cells
- Once inside the cell, protected against antibodies
- “INCLUSION BODIES” − aggregates of virus
- Basophilic − replication is complete
- Acidophilic − ongoing replication
- Intracytoplasmic – i/c – Fowl pox, vaccinia, rabies
- Intranuclear − i/n − infectious canine hepatitis
- i/c and i/n − Small pox, Canine distemper
Reactions of cells to virus
- Hyperplasia − Shope Papilloma virus
- Hyperplasia and necrosis − Fowl pox
Hyperplasia
↓
↑ Keratinisation
↓
vacuolation of cytoplasm
↓
inclusion bodies
↓
Necrosis
- Proliferation quickly followed by necrosis. e.g Vaccinia
- Necrosis alone – FMD, Rabies – Cytocidal
- Inflammatory cells - Lymphocytes, Plasma cells, Macrophages
- No neutrophils
- No suppuration
Rickettsial inflammation
- Anaplasma marginale, Ehrlichia canis, Chlamydia psittaci (intermediate between bacteria & virus)
- Obligatory parasites
- Transmitted through arthropod vectors
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Participants